2. Metabolic Enzyme/Protease Apoptosis Immunology/Inflammation Cell Cycle/DNA Damage
  3. Mitochondrial Metabolism Cytochrome P450 TNF Receptor Interleukin Related HSP LDLR Eukaryotic Initiation Factor (eIF) ClpP
  4. TBPH

TBPH is a brominated flame retardant. TBPH enhances hepatic steatosis, inflammation, and fibrosis in mice with nonalcoholic steatohepatitis (NASH). TBPH induces dysregulation of phospholipid metabolism, reducing cardiolipin (CL) and phosphatidylserine (PS) levels. TBPH leads to impaired endoplasmic reticulum-mitochondria (ER-Mito) contacts, subsequently causing mitochondrial dysfunction. TBPH induces lung injury through an inflammatory response mediated by mitochondria-derived ds-DNA. TBPH can be used to study the role of MFN2-mediated ER-mitochondria contacts in lipid metabolism homeostasis.

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TBPH

TBPH Chemical Structure

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TBPH Related Antibodies

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Description

TBPH is a brominated flame retardant. TBPH enhances hepatic steatosis, inflammation, and fibrosis in mice with nonalcoholic steatohepatitis (NASH). TBPH induces dysregulation of phospholipid metabolism, reducing cardiolipin (CL) and phosphatidylserine (PS) levels. TBPH leads to impaired endoplasmic reticulum-mitochondria (ER-Mito) contacts, subsequently causing mitochondrial dysfunction. TBPH induces lung injury through an inflammatory response mediated by mitochondria-derived ds-DNA. TBPH can be used to study the role of MFN2-mediated ER-mitochondria contacts in lipid metabolism homeostasis[1][2].

In Vitro

TBPH (5-50 μM, 48 h) promotes NASH progression by disrupting MFN2-regulated ER-Mito contacts in NASH LOs model[1].
TBPH (0-20 μg/mL, 48 h) decreases cell proliferation ability, causes oxidative stress, increase lung tissue fibrosis, causes the release of ds-DNA from lung mitochondria, which activates c-GAS-STING in TC-1 and BEAS-2B cells[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

TBPH Related Antibodies

RT-PCR[1]

Cell Line: NASH LOs model
Concentration: 5 μM, 50 μM
Incubation Time: 48 h
Result: Upregulated the transcriptional levels of oxidative stress-related genes (CYP2E1 and CYP1A2), fibrosis-related genes (COL3A1, COL4A1, LOXL2, TIMP1, VIM), and inflammation-related genes (TNF-α, IL-8).

Immunofluorescence[1]

Cell Line: NASH LOs model
Concentration: 5 μM, 50 μM
Incubation Time: 48 h
Result: Decreased colocalization of mitochondria (HSP60) and ER (GRP78), indicating reduced ER-Mito contacts.

Western Blot Analysis[1]

Cell Line: NASH LOs model
Concentration: 5 μM, 50 μM
Incubation Time: 48 h
Result: Decreased MFN2 level, increased UPRmt markers (HSP60, SOD2) and ER stress markers (GRP78, ATF6).

Western Blot Analysis[1]

Cell Line: TC-1 and BEAS-2B cells
Concentration: 0 μg/mL, 0.2 μg/mL, 2 μg/mL, 10 μg/mL
Incubation Time: 48 h
Result: Inhibited the expression of CyclinD1 and promoted the phosphorylation of Rb, increased the expression levels of CDK2/4 and P53. Increased the levels of IL-6, IL-1β, p-IκB and p-P65. Up-regulated the expression of FN and α-SMA, Down-regulated the expression of E-cadherin.
In Vivo

TBPH (20-200 mg/kg, i.g., once a day, 4 weeks) enhances hepatic lipid accumulation and metabolic dysfunction, accelerates inflammatory responses and fibrotic progression, disrupts hepatic phospholipid homeostasis and hepatocytic ER-Mito contacts, induces mitochondrial dysfunction and ER stress, in the liver in methionine-choline-deficient (MCD) diet-induced NASH mouse model[1].
TBPH (20-200 mg/kg, i.g., once a day, 4 weeks) does not alter liver morphology and does not change the hepatosomatic index, but impairs hepatocytic ER-Mito contacts, induces mitochondrial dysfunction and ER stress in normal diet (ND) mice model[1].
TBPH (0-100 μg/mL, i.g., once a day, 4 weeks) causes oxidative damage to lung cells and triggers inflammatory responses in lung cells and tissues in C57 mice[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: MCD diet-induced NASH mouse (Male C57BL/6, 8-9 weeks old, 22-25 g) model[1]
Dosage: 20 mg/kg, 200 mg/kg
Administration: i.g., once a day, 4 weeks
Result: Exacerbated hepatic pathology, increased the hepatosomatic index, enhanced lipid accumulation, decreased serum HDL and CHO levels, alongside elevated hepatic TG and serum LDL levels.
Augmented hepatic steatosis and inflammatory cell infiltration, enhanced fibrotic deposition, increased steatosis, inflammatory infiltration, fibrosis and NASH scores, elevated serum levels of AST and ALT.
Reduced the abundance of cardiolipin (CL), phosphatidylserine (PS), and phosphatidylethanolamine (PE), while increasing phosphatidic acid (PA) levels.
Disrupted lipid metabolism associated with the endoplasmic reticulum and mitochondria, altered the negative intrinsic curvature of membranes.
Reduced colocalization of ER and mitochondria in liver tissues, increased the physical distance between ER and mitochondria and reduced contact sites.
Caused a marked reduction in mitochondrial cristae, disrupted cristae junctions (CJs), and disorganization of cristae membranes in hepatocytes, reduced overall oxygen consumption and ATP content.
Increased HSP60, SOD2, mitochondrial proteases (LONP1, ClpP), GRP78, Atf6, eIF2α, and Chop levels, decreased the MFN2 protein level.
Animal Model: ND mice (Male C57BL/6, 8-9 weeks old, 22-25 g) model[1]
Dosage: 20 mg/kg, 200 mg/kg
Administration: i.g., once a day, 4 weeks
Result: Did not significantly alter liver morphology, did not change the hepatosomatic index.
Affected C14:0 metabolism, fatty acids with 13-15 carbon chains, and mitochondrial metabolic processes, altered the negative intrinsic curvature of membranes.
Reduced colocalization of ER and mitochondria in liver tissues, increased the physical distance between ER and mitochondria and reduced contact sites.
Elevated the protein levels of mitochondrial chaperone HSP60, SOD2, GRP78, Atf6, eIF2α, and Chop, decreased the MFN2 protein level.
Animal Model: C57 mice model[2]
Dosage: 0 μg/mL, 0.5 μg/mL, 1 μg/mL, 5 μg/mL, 10 μg/mL, 30 μg/mL L, 60 μg/mL, 100 μg/mL
Administration: i.g., once a day, 4 weeks
Result: Induced capillary congestion in the alveolar wall and obvious inflammatory cell infiltration. Increased the expression levels of TNFα, IL-1β, IL-6, IL-8, IFNγ, eotaxin, MCP-1, MIP-2, RANTES, p16, p21, P65, and p-IκB proteins, and decreased the expression level of cell proliferation marker (Ki67). Up-regulated the expression of FN, α-SMA, and TGF-β, down-regulated the expression of E-cadherin, and increases the content of collagen fibers in the lungs. Increased ROS and MDA levels, and decreased GSH, SOD, and CAT expression levels.
Molecular Weight

708.16

Formula

C24H36Br4O4
SMILES

O=C(OCC(CC)CCCC)C1=C(Br)C(Br)=C(Br)C(Br)C1C(OCC(CC)CCCC)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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TBPH Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

TBPHMitochondrial MetabolismCytochrome P450TNF ReceptorInterleukin RelatedHSPLDLREukaryotic Initiation Factor (eIF)ClpPCYPsTumor Necrosis Factor ReceptorTNFRILHeat shock proteinsLow-density lipoprotein receptorCaseinolytic protease PBrominated Flame RetardantNASHNASH LOs modelMFNInhibitorinhibitorinhibit

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